Cyclooxygenase (Cox) and Lipoxygenase (Lox) Gene Expression in Co-Morbidity of Pre-Eclampsia and Placental Malaria: A Case-Control Study in Korle-Bu Teaching Hospital, Ghana

Abstract

Over the years there has been an increased incidence of maternal health problems including high maternal death. Though pregnancy-related complication such as sepsis, severe bleeding, unsafe abortions, and unskilled health personnel have been implicated to this high maternal mortality rate, also the effect of hypertensive diseases such as pre-eclampsia and infectious diseases like placental malaria are major complications of pregnancy. Studies have not specifically outlined the mechanisms of pre-eclampsia aetiology and therefore it remains poorly understood. However, a multifactorial aetiology has been proposed with several risk factors. Significant numbers of studies have established an association between pre-eclampsia and placental malaria in Africa. Also, the rise in pre-eclampsia is occurring against the background of malaria infection in malaria endemic regions though malaria prevalence has decreased in recent times. Expressions of cyclooxygenase (COX) and lipoxygenase (LOX) are reported to be involved in pregnancy-related pathology such as pre-eclampsia and placental malaria. This study sought to assess whether the association between pre-eclampsia and placental malaria is through induction of either COX-1, COX-2, or 15-LOX by malaria infection. Study participants were pregnant women reporting for routine antenatal care. Using RT-PCR, we quantified the expression levels of the mRNA genes of COX-1, COX-2, and 15-LOX from placental tissue of the participants. The study established that the odds of developing pre-eclampsia are 2.09 greater for women with placental malaria compared to women without exposure, confirming the association between placental malaria and pre-eclampsia development. The study also demonstrated a significant increase in mRNA levels for COX-2 in pre-eclampsia women with placental malaria. Placental malaria could play a role in pre-eclampsia by inducing production of COX-2 leading to inflammation and consequently pre-eclampsia.